1. Volume 54, Issue 4, Pages 1166-1174 (October 1998)
Distinct contribution of Fc receptors and angiotensin II-dependent pathways in anti-GBM glomerulonephritis 
Yusuke Suzuki, Isao Shirato, Ko Okumura, Jeffrey V. Ravetch, Toshiyuki Takai, Yasuhiko Tomino, Chisei Ra 
Kidney International 
Volume 54, Issue 4, Pages (October 1998)
DOI: /j x
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2. Figure 1
Proteinuria after the injection of nephrotoxic serum in γ(-/-) mice (•), RII(-/-) (▪) mice and control wild-type (○) littermates. Each point represents the mean ± se of more than seven animals. RII(-/-) mice and control wild-type littermates (WT) were sacrificed at day 7, because they fell into lethal states. (*P < 0.01 vs. WT,‡P < 0.01 vs. RII(-/-) mice,§P < 0.01 versus WT.)
Kidney International  , DOI: ( /j x)
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3. Figure 2
Severity of glomerular damage in γ(-/-), RII(-/-) mice and control wild-type littermates (WT). Glomerular damage including endothelial swelling and vascular thrombosis in RII(-/-) (a, b and c) mice was basically as same as those of WT (d, e and f). However, these changes in RII(-/-) mice appeared earlier on day 1, and were followed by rapid progression of renal damage accompanied with cellular necrosis including mesangiolysis. In contrast, renal injuries of γ(-/-) mice before day 7 were markedly attenuated (g, h and i). Original magnification, a – i ×250.
Kidney International  , DOI: ( /j x)
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4. Figure 3
Serological changes after the injection of nephrotoxic serum in γ(-/-), RII(-/-) and control wild-type littermates (WT). (A) Blood urea nitrogen (BUN) levels; (B) serum creatinine levels. Symbols are: in A, (□) WT; (▪) γ(-/-); ▨ RII(-/-); in B, (○) WT; (•) γ(-/-); (▪) RII (-/-). Each point in both panels represents the mean ± se of more than five animals. These functional data of BUN and serum creatinine levels well reflect the severity of proteinuria and histological changes of the glomeruli in each mouse. (*P < 0.01 vs. WT,‡P < 0.01 vs. γ(-/-) mice)
Kidney International  , DOI: ( /j x)
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5. Figure 4
Histological changes of glomeruli in γ(-/-) mice at day 21 after the injection of nephrotoxic serum. (a) Light microscopy showing mesangial proliferation and glomerular enlargement as a consequence of FcR-independent mechanisms. (b) Expansion of mesangial areas was revealed by electron microscopy (*mesangial cell). (c) α-Smooth muscle actin (α-SMA) expression could be detected in mesangial cells, peripheries of Bowman’s capsules and interstitium after day 7 in addition to renal arteries and arterioles. Original magnification, a ×250, b ×2700, c ×100.
Kidney International  , DOI: ( /j x)
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6. Figure 5
Correlation between the extent of the glomerular expression of α-smooth muscle actin (α-SMA) and glomerular monocyte/macrophage (Mo/Mφ) counts in γ(-/-) mice. The glomerular expression of α-SMA was graded by semiquantitative procedure in each glomerulus (Methods section) and the average was determined as the α-SMA score of each γ(-/-) mouse. The α-SMA score was well correlated with the number of infiltrating Mo/Mφ in glomeruli (y = x; R2 = 0.948).
Kidney International  , DOI: ( /j x)
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7. Figure 6
Severity of proteinuria in γ(-/-) mice depends on the dose of the injected nephrotoxic serum. The glomerular changes observed in later stages of the disease in γ(-/-) mice appeared earlier and more severe when treated four times with nephrotoxic serum (•) rather than only once (○). Each point represents the mean ± se of more than four animals.*P < 0.05,‡P < 0.01 vs. 1 × nephrotoxic serum/γ(-/-) mice.
Kidney International  , DOI: ( /j x)
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8. Figure 7
Effects of the angiotensin II (Ang II) type 1 receptor antagonist on the severity of proteinuria in anti-GBM glomerulonephritis. Mice of each strain were divided into two groups in which the selective antagonist for Ang II type 1 receptor, TCV-116, was given 12hours before (group I) or three days after (group II) nephrotoxic serum injection. Each point represents the mean ± se of more than five mice. Symbols are: (•) γ(-/-) group I; (○) γ(-/-) group II; (▪) wild-type littermate group I; (□) wild-type littermate group II. *P < 0.01 vs. wild-type littermate group I,‡P < 0.01 vs. wild-type littermate group II,§P < 0.03 vs. γ(-/-) group II.
Kidney International  , DOI: ( /j x)
Copyright © 1998 International Society of Nephrology Terms and Conditions

9. Figure 8
Effects of the angiotensin II (Ang II) type 1 receptor antagonist on morphological changes of γ(-/-) mice in anti-GBM glomerulonephritis. A selective antagonist for Ang II type 1 receptor, TCV-116, was orally administered every day, starting 12hours before (group I), or three days after nephrotoxic serum injection. (a) Mesangial proliferation and Mo/Mφ accumulation in the glomeruli at day 21 are drastically improved in group I of γ(-/-) mice. (b) In group II of γ(-/-) mice, although transient development of renal injuries like in the untreated γ(-/-) mice are observed from day 7 to day 10, further administration of the Ang II type 1 receptor antagonist markedly reduced these changes (c) (original magnification; a, b, c ×100).
Kidney International  , DOI: ( /j x)
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10. Kidney International 1998 54, 1166-1174DOI: (10. 1046/j. 1523-1755
Kidney International  , DOI: ( /j x)
Copyright © 1998 International Society of Nephrology Terms and Conditions

11. Kidney International 1998 54, 1166-1174DOI: (10. 1046/j. 1523-1755
Kidney International  , DOI: ( /j x)
Copyright © 1998 International Society of Nephrology Terms and Conditions